<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Freiwan M</submitter><funding>Tempus Public Foundation</funding><funding>National Research, Development and Innovation Office</funding><funding>Hungarian Academy of Sciences</funding><funding>Cancer Foundation Finland sr</funding><funding>Ministry of Human Capacities</funding><pagination>2201</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8877618</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(4)</volume><pubmed_abstract>Despite the effectiveness of doxorubicin (DOXO) as a chemotherapeutic agent, dose-dependent development of chronic cardiotoxicity limits its application. The angiotensin-II receptor blocker losartan is commonly used to treat cardiac remodeling of various etiologies. The beta-3 adrenergic receptor agonist mirabegron was reported to improve chronic heart failure. Here we investigated the effects of losartan, mirabegron and their combination on the development of DOXO-induced chronic cardiotoxicity. Male Wistar rats were divided into five groups: (i) control; (ii) DOXO-only; (iii) losartan-treated DOXO; (iv) mirabegron-treated DOXO; (v) losartan plus mirabegron-treated DOXO groups. The treatments started 5 weeks after DOXO administration. At week 8, echocardiography was performed. At week 9, </pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>Investigation of the Antiremodeling Effects of Losartan, Mirabegron and Their Combination on the Development of Doxorubicin-Induced Chronic Cardiotoxicity in a Rat Model.</pubmed_title><pmcid>PMC8877618</pmcid><funding_grant_id>20391-3/2018/FEKUSTRAT</funding_grant_id><funding_grant_id>NKFIH FK129094</funding_grant_id><funding_grant_id>EFOP-3.6.3-VEKOP-16-2017-00009</funding_grant_id><funding_grant_id>Stipendium Hungaricum Scholarship</funding_grant_id><funding_grant_id>TKP2021-EGA-32</funding_grant_id><funding_grant_id>Stipendium Hungaricum Program</funding_grant_id><funding_grant_id>220015</funding_grant_id><funding_grant_id>GINOP-2.3.2-15-2016-00040</funding_grant_id><funding_grant_id>ÚNKP-21-3-SZTE-97 to M.G.K., ÚNKP-21-3-SZTE-98 to Z.Z.A.K., and ÚNKP-20-5-SZTE-166 to M.S</funding_grant_id><funding_grant_id>János Bolyai Research Fellowship</funding_grant_id><pubmed_authors>Losonczi R</pubmed_authors><pubmed_authors>Foldesi I</pubmed_authors><pubmed_authors>Sarkozy M</pubmed_authors><pubmed_authors>Dinh H</pubmed_authors><pubmed_authors>Dux L</pubmed_authors><pubmed_authors>Kovacs MG</pubmed_authors><pubmed_authors>Kovacs F</pubmed_authors><pubmed_authors>Kovacs ZZA</pubmed_authors><pubmed_authors>Horvath P</pubmed_authors><pubmed_authors>Siska A</pubmed_authors><pubmed_authors>Cserni G</pubmed_authors><pubmed_authors>Szucs G</pubmed_authors><pubmed_authors>Kriston A</pubmed_authors><pubmed_authors>Csont T</pubmed_authors><pubmed_authors>Freiwan M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Investigation of the Antiremodeling Effects of Losartan, Mirabegron and Their Combination on the Development of Doxorubicin-Induced Chronic Cardiotoxicity in a Rat Model.</name><description>Despite the effectiveness of doxorubicin (DOXO) as a chemotherapeutic agent, dose-dependent development of chronic cardiotoxicity limits its application. The angiotensin-II receptor blocker losartan is commonly used to treat cardiac remodeling of various etiologies. The beta-3 adrenergic receptor agonist mirabegron was reported to improve chronic heart failure. Here we investigated the effects of losartan, mirabegron and their combination on the development of DOXO-induced chronic cardiotoxicity. Male Wistar rats were divided into five groups: (i) control; (ii) DOXO-only; (iii) losartan-treated DOXO; (iv) mirabegron-treated DOXO; (v) losartan plus mirabegron-treated DOXO groups. The treatments started 5 weeks after DOXO administration. At week 8, echocardiography was performed. At week 9, </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2026-04-08T17:27:39.546Z</modification><creation>2025-04-19T22:38:49.513Z</creation></dates><accession>S-EPMC8877618</accession><cross_references><pubmed>35216317</pubmed><doi>10.3390/ijms23042201</doi></cross_references></HashMap>